Experimental study on Tubacin inhibiting release of inflammatory mediators in lipopolysaccharide activated microglial cells
10.3760/cma.j.issn.1671-8925.2017.04.008
- VernacularTitle:Tubacin抑制脂多糖诱导活化的小胶质细胞炎症介质释放的实验研究
- Author:
Zheng SUI
1
;
Qilong LIU
;
Guoping SUN
;
Haozhong LU
Author Information
1. 266034青岛市精神卫生中心药剂科
- Keywords:
Microglia;
Tubacin;
Histone deacetylase 6;
Inflammatory mediator;
Oxidative stress
- From:
Chinese Journal of Neuromedicine
2017;16(4):363-368
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibitory effect of T ubacin,a selective inhibition of histone deacetylase 6 (HDAC6),on the release of inflammatory mediators in lipopolysaccharide (LPS) activated microglias and its underlying mechanism.Methods BV-2 microglias were divided into control group (conventional culture),LPS group (100 ng/mL LPS),Tubacin treatment group (1 μmol/L Tubacin) and experimental group (LPS 100 ng/mL+Tubacin 1 μmol/L).The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay (ELISA).The production of nitric oxide (NO) was assayed by Griess reagent and the expression of inducible nitric oxide synthase (iNOS) was measured by Western blotting.The oxidative stress levels of BV-2 cells were determined by reactive oxygen species (ROS) and superoxide dismutase (SOD) assays.Results As compared with those in the control group,the productions of IL-6,TNF-α and NO were notably increased,the iNOS protein expression was significantly up-regulated,the ROS level was apparently elevated and the SOD activity was significantly decreased in the LPS group (P＜0.05).As compared with those in the LPS group,the productions of IL-6,TNF-α and NO were notably decreased,the iNOS protein expression was significantly down-regulated,the ROS level was apparently lessened and the SOD activity was significantly increased in the experiment group (P＜0.05).Conclusion Tubacin curbs the release of inflammatory mediators in activated microglial cells induced by LPS,whose effect may be achieved through decreasing oxidative stress levels in LPS activated microglial cells.
